Mechanism of action of Type 2 Sodium-Glucose Cotransporter Inhibitors: Beyond glycaemic control
Type 2 Sodium-Glucose Cotransporter (SGLT2) Inhibitors exercise their glucose-lowering effect through the inhibition of glucose reabsorption in the kidney. However, the cardiovascular and renal effects, as well as in those of cardiac failure, seem to occur independently from the glucose–lowering eff...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2020
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/23005
- Acceso en línea:
- https://doi.org/10.1016/j.rccar.2019.12.003
https://repository.urosario.edu.co/handle/10336/23005
- Palabra clave:
- Albumin
Sodium glucose cotransporter inhibitor
Uric acid
Adipose tissue
Antidiarrheal activity
Antihypertensive activity
Article
Cardiac muscle cell
Cell metabolism
Drug mechanism
Human
Uric acid urine level
Diabetes
Heart failure
Treatment
- Rights
- License
- Abierto (Texto Completo)
Summary: | Type 2 Sodium-Glucose Cotransporter (SGLT2) Inhibitors exercise their glucose-lowering effect through the inhibition of glucose reabsorption in the kidney. However, the cardiovascular and renal effects, as well as in those of cardiac failure, seem to occur independently from the glucose–lowering effects of these drugs. The principal mechanisms of action that explain their cardiovascular benefits are the hypotensive effect and the decrease in fill pressures, as well as direct effects on the metabolism of the myocardial cell. There is also a reduction in the urine albumin, as well as non-glycaemic effects, and a decrease in adipose tissue, with an increase in haematocrit and urine uric acid. Each one of these novel mechanisms is described in this article. © 2019 |
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